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INTRODUCTION

Rosacea is a well recognized, chronic, cutaneous condition presenting as central facial erythema, telangiectasia, papules, and pustules. A Swedish study demonstrated a prevalence of approximately 10% in the general population.1 In the United States, it is believed that there are 13 million people affected with rosacea. It is usually diagnosed between the ages of 30 and 50 years and although both genders can be affected, it is more common in women, with more men experiencing the phymatous changes. Rosacea is also more prevalent in fair-skinned than dark-skinned individuals. Sun damage, a propensity to flush, and genetic predisposition are risk factors in acquiring rosacea.

ETIOLOGY

The precise causal pathway of rosacea still remains unknown. In addition to genetic predisposition, many other factors have been implicated in the pathogenesis of rosacea. These include Demodex folliculorum mites, Helicobacter pylori infection, vascular lability, response to chemical and ingested agents, and psychogenic factors. Sunlight, heat, alcohol consumption, and spicy food are also very well known for their contributions in aggravating rosacea symptoms. The association of rosacea and digestive tract bacteria is controversial. Helicobacter pylori is a very common infection of the digestive tract and there are studies supporting both sides of the argument.2–4 It has been suggested that intestinal inflammation5 and bacteria may cause hypersensitization of facial sensory neurons via the plasma kallikrein–kinin pathway and production of bradykinin, a well-known vasodilator6 (Box 16-1).

BOX 16-1

The kinin-kallikrein system or “kinin system” is a poorly delineated system of blood proteins that plays a role in inflammation, blood pressure control, coagulation, and pain. Its important mediators, bradykinin and kallidin, are vasodilators.

Rosacea is associated with dermal connective tissue damage and pilosebaceous abnormalities. The follicular immune response observed in rosacea has led some authors to suggest that the pilosebaceous inflammation secondary to Demodex mites and bacteria are the key to developing rosacea.7,8 Although the potential involvement of Demodex mites in rosacea still remains controversial, matrix metalloproteinase-9 (MMP-9), also known as gelatinase, has been implicated with somewhat more confidence in the pathophysiology of this condition. Increased levels of MMP-9, if not controlled by its inhibitors, result in an inflammatory response and the degradation of collagen. Afonso et al. demonstrated that MMP-9 is increased in patients with ocular rosacea.9 In addition, the expression of MMP-9 has been shown to be increased in the fibroblasts of patients with Demodex folliculorum and rosacea when compared to patients with rosacea in the absence of Demodex mites.10 More research is warranted to study the correlation between Demodex mites and MMPs in the etiology of rosacea.

Another leading theory is based on vascular response. Flushing and telangiectasias are major symptoms in patients affected with rosacea. A combination of superficiality of cutaneous vasculature on the face,11 higher blood flow of facial skin,12 and vascular dysregulation via humoral and neural mechanisms13...

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